Cases reported "Osteomalacia"

Filter by keywords:



Filtering documents. Please wait...

1/10. IgA-kappa type multiple myeloma affecting proximal and distal renal tubules.

    A 45-year-old male was admitted because of chest pain, lumbago, and bilateral ankle pain. Examination disclosed hypophosphatemic osteomalacia, acquired fanconi syndrome, and abnormalities in distal nephron such as distal renal tubular acidosis and renal diabetes insipidus. Further exploration revealed IgA kappa multiple myeloma excreting urinary bence jones protein (kappa-light chain). Renal biopsy revealed thick basement membranes and elec-tron-dense crystals in proximal tubular epithelial cells. Immunofluorescent studies revealed deposition of kappa-light chain in renal tubular epithelial cells that caused the renal tubular damage. Although the osteomalacia was relieved by medical treatment, the urinary bence jones protein and the renal tubular defects were not improved by the chemotherapy for the myeloma. The patient died of exacerbation of multiple myeloma at 50 years of age.
- - - - - - - - - -
ranking = 1
keywords = tubule
(Clic here for more details about this article)

2/10. Hypophosphatemic rickets and osteomalacia in polyostotic fibrous dysplasia.

    A 17 year-old girl with polyostotic fibrous dysplasia and hypophosphatemia had inappropriately low tubular reabsorption of phosphate. She had radiological evidence of rickets and osteomalacia. The patient showed clinical improvement after treatment with phosphate supplementation, active vitamin D (calcitriol) and alendronate. It is postulated that either a phosphaturic substance elaborated from the dysplastic bone or target-organ (kidney) unresponsiveness may interfere with phosphate reabsorption in the renal tubule.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

3/10. Oncogenous osteomalacia: a case study.

    A case of oncogenous osteomalacia due to a fibrosarcoma of the maxilla is reported, with a 19 year course before treatment. Metabolic studies of calcium and phosphorus were performed 3 and 19 years after the first symptomology. There was a negative balance for both phosphorus and calcium with low serum levels of 1,25-dihydroxyvitamin D which were corrected by resection of the tumor. Portions of the tumor were cultured and the supernatant did not affect phosphorus transport by a proximal tubule kidney cell line. Other portions were injected into athymic nude mice where they resulted in hypophosphatemia and phosphaturia, thus confirming the endocrine nature of the oncogenous osteomalacia factor.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

4/10. hemangiopericytoma-induced osteomalacia: tumor transplantation in nude mice causes hypophosphatemia and tumor extracts inhibit renal 25-hydroxyvitamin D 1-hydroxylase activity.

    Although more than 50 patients with the tumor-induced osteomalacia syndrome, characterized by remission of unexplained osteomalacia after resection of a coexisting tumor, have been reported, the pathogenesis of this syndrome is still not clear. We investigated the cause of biopsy-confirmed osteomalacia which was resistant to treatment with 1 alpha-hydroxyvitamin D3 in a 54-yr-old man. He had severe hypophosphatemia, a high serum alkaline phosphatase level, a low plasma 1,25-dihydroxyvitamin D level, and remarkably increased urinary phosphorus excretion. A tumor, with histological characteristics of a hemangiopericytoma, was found on his left thigh. After surgical removal of this tumor, his plasma 1,25-dihydroxyvitamin D and serum phosphorus levels increased to normal levels, and his bone pain subsided. The tumor was transplanted to athymic nude mice. A nodule formed in each mouse, with histological features identical to those of the original tumor, and the tumor-bearing mice had hypophosphatemia, high serum alkaline phosphatase levels, and increased urinary phosphorus excretion. When extracts of the original tumor were added to primary cultures of renal tubular cells, renal cAMP levels did not change, but 25-hydroxyvitamin D-1 alpha-hydroxylase activity was significantly inhibited. These data indicate tumoral production of some humoral factor(s) inhibiting 25-hydroxyvitamin D-1 alpha-hydroxylase activity and phosphorus reabsorption unrelated to adenylate cyclase-cAMP production in proximal renal tubules.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

5/10. cadmium-induced osteopathy: clinical and autopsy findings of four patients.

    Clinical and autopsy findings of 4 patients with chronic cadmium toxication by peroral uptake of cadmium are reported. cadmium toxication was liable to occur in multiparous postmenopausal women, and it began with proteinuria, glycosuria, lumbago and bone pain. Then, renal function gradually decreased being accompanied with renal tubulopathy. autopsy disclosed renal tubulopathy, which consisted of the flattening of the epithelium of proximal convoluted tubules at the peripheral portion and the mild thickening of the tubular basement membrane. There was no primary change in the glomerulus and renal interstitium. osteomalacia was observed in the vertebrae and several other bones. The degree of osteomalacia was in good agreement with chronic renal tubular dysfunction. A decrease of the estrogen content, in addition to renal tubulopathy due to biological saturation of cadmium, seems to play an important role in the pathogenesis of cadmium-induced osteomalacia.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

6/10. Albright's syndrome with rickets.

    Four patients are reported who had Albright's syndrome, hypophosphatemia, and inappropriately low renal tubular reabsorption of phosphate. Three of the patients had radiologic evidence of rickets or osteomalacia, and the fourth had a bone biospy, which showed microradiographic evidence of a previous mineralization defect. serum parathormone values were elevated before treatment in two patients. Intravenous infusions of calcium in one patient, and of calcium and parathormone in a second patient, showed appropriate target-organ responsiveness. patients generally showed radiologic improvement of rickets after treatment with large doses of vitamin D, but such treatment failed to restore normal serum values of phosphorus and alkaline phosphatase. It is postulated that a substance elaborated from the dysplastic bone may be interfering with phosphate reabsorption in the renal tubule.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

7/10. Renal responsiveness to parathyroid hormone in a case of nonfamilial hypophosphatemic osteomalacia.

    plasma immunoreactive parathyroid hormone level, urinary excretion of adenosine cyclic 3',5'-monophosphate (cyclic amp) and the sensitivity of the renal tubule to calcium infusion and to parathyroid extract were investigated in a patient with nonfamilial hypophosphatemic osteomalacia. plasma immunoreactive parathyroid hormone concentration was normal and basal urinary excretion of cyclic amp was increased. Renal cortical adenylate cyclase, as measured by urinary cyclic amp excretion, was certainly as sensitive to exogenous parathyroid extract as in normal subjects. After a previous calcium infusion, a greater parathyroid-hormone-sensitive component of phosphorus transport in the kidney was present than in two control subjects. Our results indicate that in nonfamilial hypophosphatemic osteomalacia the renal tubule could be hyperresponsive to parathyroid hormone.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

8/10. cadmium-induced osteomalacia.

    The detailed study of a battery plate maker, who had worked with cadmium for 36 years, showed that proteinuria, typical of renal tubular dysfunction, had been observed for 25 years and during the last 12 years of his life the patient had suffered increasing disability from gross bone disease. Several bone biopsies and detailed metabolic studies showed typical severe osteomalacia, which responded well initially to calcium and vitamin D treatment. Examination of the liver both in life and after death showed a gross excess of cadmium. This was also found in the kidneys after death. Previously unreported changes were present in the bones, especially the lumbar vertebrae which were probably more the result of gross bone deformity than cadmium deposition. The mechanism of development of the severe acquired fanconi syndrome was thought to be a combination of dietary calcium and vitamin d deficiency and impaired calcium absorption from abnormal vitamin D synthesis, related to the cadmium deposition in the renal tubules, which also caused the defect in renal tubular reabsorption.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

9/10. osteomalacia as a presenting manifestation of sjogren's syndrome.

    osteomalacia is still common in morocco, where the leading causes are nutritional deficiencies followed by intestinal diseases. osteomalacia rarely occurs as the first manifestation of a renal tubule disorder due to a connective tissue disease such as sjogren's syndrome. The case of a 40-year-old woman who presented with a five-year history of generalized bone pain, severe weight loss and a waddling gait is reported. She had low levels of serum phosphate (0.74 mmol/L), serum calcium (1.97 mmol/L), and urinary calcium (1.22 mmol/24 h). serum alkaline phosphatase was 210 IU/L. Roentgenograms showed Looser's zones (right femoral neck, sixth and seventh right ribs). There was bilateral parotid gland enlargement, dryness of the mouth, nose and eyes, and bilateral punctate keratitis. A lip biopsy showed changes corresponding to stage II of the Chisholm and Mason classification. Tests for rheumatoid factor (latex and Waaler-Rose) and antinuclear factor were negative. The alkaline reserve was 18 mmol/L, serum potassium was 3.5 mmol/L, serum chloride was 112 mmol/L and urinary pH was 6.5. A renal biopsy showed tubulointerstitial lesions, lymphoplasmocytic infiltrates and interstitial sclerosis with patchy tubular atrophy. The patient was given bicarbonates, high-dose vitamin D followed by 1-alpha-hydroxycholecalciferol (0.3 microgram/d), and calcium (1 g/d). Follow-up was 42 months at the time of this writing. The role of tubular disorders in the genesis of osteomalacia is discussed, and the renal manifestations of sjogren's syndrome are reviewed.
- - - - - - - - - -
ranking = 0.25
keywords = tubule
(Clic here for more details about this article)

10/10. Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D production in renal tubules.

    A 60-year-old man with portal hypertensive gastropathy due to type C liver cirrhosis developed severe bone pains, marked hypophosphatemia with inappropriately increased urinary excretion of phosphate (%TRP; 9.6%), and hyperalkaline phosphatasia, after intravenous administration of saccharated ferric oxide (SFO) at a dose of 80-240 mg/week over a period of more than 5 years. The total iron infused was estimated to be more than 25 g. On a diagnosis of SFO-induced osteomalacia, the infusion of iron was immediately discontinued, and phosphate and vitamin D2 (1000 IU/day) were administered. serum levels of 25-OHD2 increased after 1 week, whereas levels of 1,25-(OH)2D2 did not increase until 3 months later, accompanied by improvement of renal tubular reabsorption of phosphate and gradual improvement of the bone pains. The patient has been doing well for the last 2 years, with normal serum levels of phosphate, calcium, and alkaline phosphatase, without any supplementation of phosphate, vitamin D, or iron-containing agents. In primary culture of neonatal mouse renal tubules, in which 1,25-(OH)2D3 was produced from 25-OHD3 in response to PTH, SFO significantly inhibited PTH-induced production of 1,25-(OH)2D3 at 30 mumol/L, which is attainable in the urine of patients receiving a therapeutic intravenous dose of SFO. Furthermore, SFO decreased the calcium content and inhibited 45Ca incorporation in cultured fetal mouse parietal bones at 3 mumol/L. Such SFO concentration may be transiently observed in the plasma of patients receiving excessive intravenous doses of SFO for a prolonged period. These in vitro findings together with the clinical observations suggest that SFO, after filtration through the glomerulus and reabsorption in the proximal renal tubules, impaired proximal renal tubular function, such as tubular reabsorption of phosphate and 1 alpha-hydroxylase activity, leading to hypophosphatemic osteomalacia. Furthermore, it is highly likely that SFO in the peripheral blood, when transferrin is saturated with iron, may impair bone formation and aggravate osteomalacia. Although SFO-induced osteomalacia is reversible simply by discontinuation of the agent, excessive and prolonged administration of SFO should be avoided.
- - - - - - - - - -
ranking = 1.5
keywords = tubule
(Clic here for more details about this article)
| Next ->


Leave a message about 'Osteomalacia'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.